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Your Environment. Your Health.

Progress Reports: Duke University: Persistent Mitochondrial and Epigenetic Effects of Early Life Toxicant Exposure

Superfund Research Program

Persistent Mitochondrial and Epigenetic Effects of Early Life Toxicant Exposure

Project Leader: Joel N. Meyer
Co-Investigators: Susan K. Murphy, Theodore A. Slotkin (Duke University Medical Center)
Grant Number: P42ES010356
Funding Period: 2017-2022
View this project in the NIH Research Portfolio Online Reporting Tools (RePORT)

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Progress Reports

Year:   2019  2018  2017 

A multitude of mitochondrial diseases are caused by genetic differences in genes that encode proteins that protect mitochondria. However, some people who have these genetic differences are more affected than others. Joel Meyer, Ph.D., and his team found that these differences sensitize nematodes used in the project to certain exposures (Hartman et al., 2019), suggesting that people with these disease genes may also be at greater risk than the rest of the population. If this is true in people as well as in the project’s nematode model, this information can help the team protect people more effectively. However, the researchers also found that genetic sensitivity to arsenic, a common contaminant of drinking water across the globe, is also dependent on the age at which exposure occurs (Hershberger et al., 2019). In a collaborative effort, the team also built new tools for the analysis of behavior in the project’s nematode model (Smith et al., 2019), as well as for manipulating and imaging these near-microscopic animals (Bachman et al., 2019; Zhang et al., 2019). These efforts will facilitate future toxicological studies with this alternate model, which permits faster and cheaper analysis of chemical toxicity compared to traditional mammalian models.

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